The goals of this project are to characterize the host's immune response to helminth infections and to relate the findings to protective immunity and the pathogenesis of clinical disease. In filariasis susceptibility to infection appears partially genetically determined but unrelated to HLA. Experimental evidence indicates that IgE antibodies are important in protective immunity, and these antibodies are being quantified and immunologically characterized. IgE antibodies also appear to play a pathogenetic role in initiating inflammatory (allergic) reactions in tropical eosinophilia and may contribute along with immune complexes to the lymphatic inflammation leading to elephantiasis. Chronic helminth infections are characterized by intense modulation of the host response to parasite antigens. Humoral and cellular suppressive mechanisms regulate lymphocyte responsiveness in human schistosomiasis and filariasis and IgG blocking antibodies have been found to modulate immediate hypersensitivity responses. Following specific treatment the effects of these suppressive mechanisms is either diminished or lost. Eosinophils are prominent in the host response to helminth infections. Purification of these autofluorescent cell by flow microfluorometry has permitted in vitro studies of their anti-parasite killing properties.